Eye Review Flashcards

1
Q

Label the illustration

A
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2
Q

How should an eye review Hx be structured?

A

HOPC (unilateral or bilateral eye problem)

PMHx

Past ocular Hx

FHx

SHx

Rx

Allergies

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3
Q

Outline the structure of the eye exam

A

VISION, PUPILS, PRESSURE

1) Visual acuity + further examinations according to suspected Dx (e.g. pin hole, contrast sensitivity, colour saturation, Ishihara colour vision test, visual fields by confrontation, light saturation)
2) Pupil reactions: direct, consensual, swinging
3) IOP + additional tests (e.g. corneal reflections, EOMs, cover testing, corneal sensation, red reflex)
4) Slit lamp/fundus examination

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4
Q

How is visual acuity measured?

A

Using a Snellen chart

Patient is positioned at a predetermined distance from the chart (classically 6 metres) in well illuminated room and covers one eye at a time

Try pinhole if VA is 6/9 or worse

NB Leave distance glasses/bifocals/multifocals on for the test but take reading glasses off

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5
Q

How is contrast sensitivity assessed?

A

Using a Pelli-Robson contrast sensitivity chart

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6
Q

How can colour saturation be tested?

A

Ask patient to cover one eye (start by covering “bad eye” if you already know which this is) and look at something red

Then ask them to swap eyes and report any change

“If the intensity of the colour in one eye is worth $1, how much is it worth in the other eye?” E.g. 30 cents in this example

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7
Q

How can colour vision/differentiation be assessed?

A

Using Ishihara colour plates

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8
Q

How can light saturation be tested?

A
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9
Q

How is the swinging light test performed and how are the findings interpreted? What does it assess for?

A

Assesses for RAPD

Swing the light between the two eyes; the pupil with the poorer, functioning anterior visual pathway will dilate despite light stimulus

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10
Q

Describe the light reflex pathway

A
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11
Q

What is the Marcus Gunn pupil?

A

RAPD

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12
Q

What is the Argyll Robertson pupil?

A

Pupil constricts on accommodation (when focussed on an object close-up) but NOT to light

Highly specific sign of neurosyphilis, and may also be a sign of diabetic neuropathy

In general, pupils that “accommodate but do not react” are said to show light-near dissociation - i.e., it is the absence of a miotic reaction to light, both direct and consensual, with the preservation of a miotic reaction to near stimulus (accommodation-convergence)

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13
Q

What is the Holmes Adie pupil?

A

Tonically dilated pupil that does not react to light

Associated with damage to parasympathetic pupillary fibres

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14
Q

How is IOP measured?

A

By applying pressure to the cornea using a tono-pen or Goldmann applanation tonometry; IOP is inferred from the force required to “flatten” (applanate) the cornea

Topical anaesthetic should be applied to the eye first to reduce discomfort caused by probe making contact with the cornea

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15
Q

What influences IOP? What is its normal range?

A

Measurement is influenced by corneal thickness (i.e. a thicker cornea will have more resistance and produce a higher IOP reading)

Normal IOP: 6-21mmHg (mean 15mmHg)

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16
Q

How may visual fields be tested?

A

By confrontation

By automated perimetry (uses a mobile stimulus moved by a perimetry machine; patient indicates whether he sees the light by pushing a button)

Using an Amsler grid (used to detect visual field defects within the centremost region of the visual field)

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17
Q

How are results of visual field testing recorded?

A

Documentation is from the patient’s point of view

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18
Q

What do positive findings on Amsler grid testing usually indicate?

A

Macular pathology

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19
Q

What might abnormal EOMs indicates?

A

Cranial nerve palsy (III, IV, VI)

Muscle entrapment (e.g. in orbital #)

Muscle infiltrate (e.g. thyroid eye disease)

Muscle weakness (i.e Guillain-Barre Miller-Fisher variant)

Gaze centre dysfunction (e.g. horizontal gaze palsy, internuclear opthalmoplegia)

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20
Q

Internuclear opthalmoplegia

A

Disorder of conjugate lateral gaze in which the affected eye shows impairment of adduction

Caused by injury or dysfunction in the medial longitudinal fasciculus (MLF); in young patients with bilateral INO, multiple sclerosis is often the cause and in older patients with one-sided lesions a stroke is a distinct possibility

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21
Q

Miller Fisher variant of GBS

A

Rare, acquired nerve disease characterised by abnormal muscle coordination, paralysis of the eye muscles, and absence of the tendon reflexes; like Guillain-Barré syndrome, symptoms may be preceded by a viral illness

Majority of individuals with Miller Fisher syndrome have a unique antibody that characterises the disorder

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22
Q

How is corneal reflection testing (Hirschberg test) performed?

A

By shining a light in the person’s eyes and observing where the light reflects off the corneas

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23
Q

6 causes of leukocoria

A

Cataract

Retinoblastoma

Coats’ disease

Retinal detachment

Retinopathy of prematurity

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24
Q

How is the red reflex tested?

A

The red reflex refers to the reddish-orange reflection of light from the eye’s retina that is observed when using an ophthalmoscope or retinoscope from approximately 30 cm / 1 foot; examination is usually performed in a dimly lit or dark room

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25
Q

How is cover testing performed and how are results interpreted?

A

Unilateral cover test is performed by having the patient focus on an object then covering the fixating eye and observing the movement of the other eye; if the eye was exotropic, covering the fixating eye will cause an inwards movement, and esotropic if covering the fixating eye will cause an outwards movement

Dominant fixating eye being covered prompts the other eye to take up fixation (see image)

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26
Q

What is the purpose of cover testing?

A

Used to determine both the type of ocular deviation and measure the amount of deviation; two primary types of ocular deviations are the tropia and the phoria

Tropia is a misalignment of the two eyes when a patient is looking with both eyes uncovered; a phoria (or latent deviation) only appears when binocular viewing is broken and the two eyes are no longer looking at the same object

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27
Q

What is leukocoria?

A

An abnormal white reflection from the retina of the eye (seen in place of the normal red reflex)

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28
Q

What is Coats’ disease?

A

Coats’ disease (AKA exudative retinitis or retinal telangiectasis) is a rare congenital, nonhereditary eye disorder, causing full or partial blindness, characterized by abnormal development of blood vessels behind the retina

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29
Q

How should the slit lamp examination be approached?

A

Examine from superficial to deep structures:

Lids

Tear film

Conjuctiva

Episclera and sclera

Cornea

Anterior chamber

Iris

Pupil

Lens

Fundus examination

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30
Q

Explain how a fundal assessment should be performed

A

Dark room, comfortable position for the patient

Ask patient to look into the distance (accommodation constricts the pupil)

Use your R eye for the patient’s R eye and your L eye for the patient’s L eye

Hand on the patient’s forehead allows you to stabilise the distance between the patient’s fundus and fundoscope

Using the dial: green numbers (+) shortens the focal length of the fundoscope and red numbers (-) increase

Once you have the retina in focus, try following a blood vessel to the optic disc

Disc is on nasal side of retina

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31
Q

Revise your fundal anatomy!

A
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32
Q

What do each of these illustrations demonstrate?

A
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33
Q

How can myopia and hypermetropia be corrected?

A
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34
Q

What is astigmatism? What is regular vs irregular astigmatism and what are the implications for Mx?

A

Normal cornea is curved like a sphere

Regular astigmatic cornea has 2 different curves at 90 degrees to each other and is correctable with glasses or contact lenses

Irregular astigmatic cornea has variable degrees of curvature along each axis and is not easily corrected with glasses-

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35
Q

What is the fastest way to detect a refractive error and how does this work?

A

Pinhole; obscures the light which has been inappropriately focussed onto the retina

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36
Q

What is presbyopia and how is it managed?

A

Long-sightedness caused by loss of elasticity of the lens of the eye, occurring typically in middle and old age (lens loses its flexibility with age)

Mx: reading glasses/bifocals

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37
Q

Main causes of cataracts

A

Age-related

Drugs (e.g. steroids)

Trauma (including intra-ocular surgery)

Systemic diseases (e.g. DM, myotonic dystrophy, Wilson’s disease, atopic dermatitis)

Ocular diseases (e.g. uveitis, retinitis pigmentosa)

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38
Q

Sx of cataracts

A

Gradual decrease in visual acuity and increase in glare Sx over weeks to years

39
Q

How is cataract surgery performed? What is the success rate?

A

Patients often admitted as day case

Usually performed under topical or local anaesthesia

Patient must be able to lie flat and still

Approach: phacoemulsification (emulsification and aspiration of the lens) with insertion of intra-ocular lens

Post-op Abx and steroid eye drops prescribed over 4 weeks

Post-op r/vs at 1 day, week and month

Success rates: visual improvement in >95% of operations performed

40
Q

What is a cataract?

A

Clouding of the lens in the eye leading to a decrease in vision

41
Q

Describe the movement of aqueous humor through the anterior chamber

A
42
Q

What are the 3 major clinical features of POAG?

A

Progressive visual field loss

Progressive increase in cup-to-disc ratio of optic disc

Elevated IOP

NB Some people have high IOP but no evidence of glaucoma (ocular HTN), some people have features of glaucoma despite normal IOP (normal tension glaucoma)

43
Q

How does visual loss progress in glaucoma?

A
44
Q

If the L image is a normal optic disc, what is the pathology on the R?

A

Increased cup to disc ratio seen in glaucoma

45
Q

What is the aim of medical Mx for POAG?

A

To lower IOP and slow disease progression by increasing aqueous outflow or decreasing aqueous production

Lowering IOP slows disease progression, even when IOP is already in normal range

46
Q

Eye drops for POAG; give an example of each

A

Prostaglandin inhibitors: latanoprost (Xalatan)

Beta blockers: timolol (timoptic)

Alpha agonists: brimonidine (Alphagan)

Miotics: pilocarpine

Carbonic anhydrase inhibitors: brizolamide (Azopt)

47
Q

Tablets for treatment of POAG

A

Carbonic anhydrase inhibitors: acetazolamide (Diamox)

48
Q

Mechanism of action of prostaglandin inhibitors for Mx of POAG

A

Increase aqueous outflow

49
Q

Mechanism of action of B blockers for Mx of POAG

A

Decrease aqueous production

50
Q

Mechanism of action of alpha agonists for Mx of POAG

A

Increase aqueous outflow AND decrease production

51
Q

Mechanism of action of miotics for Mx of POAG

A

Increase aqueous outflow

52
Q

Mechanism of action of carbonic anyhydrase inhibitors for Mx of POAG

A

Decrease aqueous production

53
Q

Mx of POAG

A

Medical: eye drops, tablets

Laser: selective laser trabeculoplasty (SLT; this is a good alternative for pts who do not tolerate or comply with daily eye drops)

Surgical: trabeculectomy (creation of an alternative drainage path for aqueous through the formation of a subconjunctival bleb)

54
Q

Describe the pathophysiology of uveitic glaucoma

A

Synechiae (“adhesions”) and inflammatory cells effect fluid dynamics within the anterior chamber

55
Q

Describe the pathophysiology of neovascular glaucoma

A

Neovascularisation of angle leads to reduced drainage of aqueous humor and increased IOP

Neovascularisation occurs secondary to ischaemia in the eye (e.g. in setting of central retinal vein occlusion, CRVO, or proliferative diabetic retinopathy)

Leads to characteristic “rubeosis iridis” appearance (new blood vessels seen on surface of iris

56
Q

How is non-proliferative diabetic retinopathy graded? What findings are seen with each grading?

A

Mild NPDR: microaneurysms

Moderate NDPR: microaneurysms, intra-retinal haemorrhages, hard exudates, cotton wool spots

Severe NPDR (any one feature of the “4-2-1 rule”): intra-retinal haemorrhages in 4 quadrants, OR venous beading in 2 quadrants, OR IRMA (intra-retinal vascular abnormalities) in 1 quadrant)

Very severe NPDR: 2 features from the 4-2-1 rule

57
Q

How can retinal microaneurysms be better visualised?

A

Using fluorescain angiography

58
Q

Features of mild NPDR

A

Microaneurysms

59
Q

Features of moderate NPDR

A

Microaneurysms

Intra-retinal haemorrhages

Hard exudates

Cotton wool spots

60
Q

Severe NPDR

A

Any one of:

Intra-retinal haemorrhages in 4 quadrants

Venous beading in 2 quadrants

IRMA in 1 quadrant

NB If 2 features, this is classified as very severe NPDR

61
Q

What is proliferative diabetic retinopathy?

A

Advanced form of diabetic eye disease that occurs when blood vessels in the retina disappear and are replaced by new fragile vessels that bleed easily; can result in sudden loss of vision

62
Q

Distinguish between low- and high-risk PDR

A

Low: <1/3 of disc neovascularised (NVD)

High: NVD plus vitreous haemorrhage, OR NVD >1/3 of disc, OR NVE (neovascularisation everywhere!)

63
Q

How is PDR managed?

A

Pan-retinal photocoagulation; burns away areas of peripheral retina, decreases drive of VEGF production (leading to reduced neovascularisation), with sacrifice of peripheral vision

64
Q

What processes can cause diavetic maculopathy?

A

Macular oedema

Macular ischaemia

65
Q

Mechanism of macular oedema in diabetic maculopathy

A

Leakage of fluid into foveal tissue

Lipid exudates adjacent to fovea

66
Q

Mechanism of macular ischaemia in diabetic maculopathy

A

Capillary non-perfusion at fovea

67
Q

What sign on fluorescein angiography indicates macular ischaemia?

A

Enlarged foveal avascular zone and capillary drop-out

68
Q

How can macular oedema be visualised?

A

Using optical coherence tomography (OCT), a non-invasive imaging test that uses light waves to take cross-section pictures of your retina, the light-sensitive tissue lining the back of the eye

Shows fluid leakage and lipid exudates adjacent to fovea

69
Q

Mx of diabetic macular oedema

A

Macular (grid) laser

Intra-vitreal anti-VEGF agents

70
Q

Mx of macular ischaemia

A

No specific treatment: BSL control, BP control, cholesterol control

71
Q

What is the most common cause of blindness in people >50 in the developed world?

A

Dry age-related macular degeneration

72
Q

Major risk factors for dry macular degeneration

A

Increasing age

Smoking

73
Q

Mx for dry macular degeneration

A

Amsler grid: frequent use allows patient to detect changes/new distortion of vision

Cessation of smoking

Low vision aids

74
Q

Appearance of dry macular degeneration on fundoscopy and OCT

What is drusen?

What is geographic atrophy?

A

Drusen are yellow lipid deposits under the retina; while drusen likely do not cause age-related macular degeneration (AMD), their presence increases a person’s risk of developing AMD

Geographic atrophy is the advanced (late) form of dry AMD; atrophy refers to the degeneration of the deepest cells of the retina (retinal pigment epithelium; RPE), which normally helps maintain the photoreceptor cells

75
Q

What is the classic feature of wet (neovascular) age-related macular degeneration?

A

Choroidal neovascularisation (CNV): abnormal new vessels grow from choroid to RPE (process linked to increased VEGF levels), and these vessels bleed/leak, leading to macular scarring

76
Q

Mx of wet macular degeneration

A

Anti-VEGF agents via (typically monthly) intra-ocular injection: ranbizumab, bevacizumab

Photodynamic therapy

Macular laser

77
Q

Photodynamic therapy (PDT)

A

Photodynamic therapy (PDT) is a treatment that uses a drug, called a photosensitizer or photosensitizing agent, and a particular type of light; when photosensitizers are exposed to a specific wavelength of light, they produce a form of oxygen that kills nearby cells

78
Q

What is the classical appearance of a 3rd nerve palsy?

A

“Down and out”

79
Q

What are the major causes of CN III palsy?

A

Compressive: from tumour, haemorrhage or aneurysm (commonly pupil involving)

Vascular: HTN, DM (commonly pupil sparing)

Trauma

Vasculitis (i.e. GCA)

Demyelinating disease

Idiopathic

80
Q

Ix of CN III palsy

A

MRI/MRA urgently if compressive lesion suspected

BP and blood tests for vascular risk factors (including glucose, lipid profile)

81
Q

Mx and prognosis of CN III palsy

A

According to the cause

Prognosis is variable

82
Q

Classic appearance of a CN IV palsy

A

Tip, turn and tilt

83
Q

Causes of CN IV palsy

A

Trauma (can cause bilateral CN IV involvement)

Microvascular disease

Tumour

Demyelination

Vasculitis (GCA)

Idiopathic

Can be congenital

84
Q

Ix for CN IV palsy

A

Old photos (if congenital palsy suspected)

Bloods for vascular risk factors

Consider neuro-imaging

85
Q

Mx of CN IV palsy

A

According to cause

Prisms in glasses +/- strabismus surgery to re-align the visual axis if not improving

86
Q

Strabismus

A

Abnormal alignment of the eyes

87
Q

What kind of difficulties are experienced by the patient with CN IV palsy and why?

A

SO allows eye to look down, inwards and provides intortion

A CN IV palsy can cause difficulty reading and walking down stairs

88
Q

Classic appearance of a CN VI palsy

A

Abduction deficit

89
Q

What Sx will a patient complain of with a CN VI palsy?

A

Horizontal diplopia (binocular)

90
Q

Causes of CN VI palsy

A

Vascular

Raised ICP

Tumours

Trauma

Demyelinating disease

Vasculitis (GCA)

Idiopathic

91
Q

DDx for underlying cause in CN VI palsy

A

Thyroid eye disease

Medial wall blow-out #

Myaesthenia gravis

92
Q

Ix of CN VI palsy

A

Assess vascular RFs

MRI if other associated pathology present, if palsy does not resolve in 3/12 or if patient <40

93
Q

Mx of CN VI palsy

A

According to cause

Prisms +/- strabismus surgery

Botox to ipsilateral MR

94
Q

Interpretation of visual fields

A